"We provide evidence that the small molecule binds to both cellular and viral membranes, but its preferential ability to inactivate viral membranes comes from its ability to exploit the biogenic reparative ability of metabolically active cells versus static viral membranes," he said. "That is, at antiviral concentrations, any damage it does to the cell's membrane can be repaired, while damage done to static viral membranes, which have no inherent regenerative capacity, is permanent and irreversible."

Lee and his collaborators developed their concept of LJ001 as interfering only with enveloped viruses after testing 23 pathogens in cell culture. Studies of nine of those agents - including Ebola virus, Nipah virus and Rift Valley fever virus - required high- or maximum-containment facilities and were carried out in the biosafety level 3 and 4 laboratories of the University of Texas Medical Branch at Galveston (UTMB) and USAMRIID.

"Once we started testing more and more, we figured out that it was only targeting the enveloped viruses," said Alexander N. Freiberg, director of UTMB's Robert E. Shope, M.D., Laboratory.

The Shope BSL4 lab was also used for mouse experiments with Ebola and Rift Valley fever virus that further confirmed the protective value of LJ001.

While the exact mechanism of viral membrane inactivation is unknown, the researchers are pursuing some promising leads that could answer that question.

Additionally, the drug does not appear to be toxic in vitro or in animals when used at effective antiviral concentrations.

UCLA has filed for a patent on the use of the compound. The study is available in Proceedings of the National Academy of Sciences at pnas/content/early/2010/01/27/0909587107.